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. 2019 Oct 4;116(10):1742–1755. doi: 10.1093/cvr/cvz251

Figure 2.

Figure 2

Cardiac-specific Trx1 deletion induces failing heart phenotypes. (A) H&E stained images of samples from Trx1cKO mice at 6 days of age. (B) Representative M-mode echocardiography images taken from Trx1cKO mice at 4 weeks of age. WT, wall thickness’ LVEDD, LV end diastolic dimension; LVESD, LV end systolic dimension; DSEP, diastolic septal; DP, diastolic posterior; SP, systolic posterior; SSEP, systolic septal. (C) Contractile dysfunction in Trx1cKO mice. Ejection fraction, an index of cardiac contractile function, was determined by echocardiographic analysis. (D) Lung congestion, characterized by lung weight/tibia length ration, is induced in Trx1cKO mice. (E) Cardiac hypertrophy, characterized by heart weight/tibia length ratio, is induced in Trx1cKO mice. (F) WGA (wheat germ agglutinin) staining was performed to assess cardiomyocyte size in Trx1cKO mice. (G) Cardiac fibrosis in Trx1cKO mice. Representative PASR staining. Relative cardiac fibrosis was measured using the ImageJ program. (H) Increased apoptotic cell death in Trx1cKO mice. TUNEL staining was performed in Trx1cKO mice. (I) Increased cleaved caspase 3 in Trx1cKO mice. The numbers of mice examined in each experimental group were: 5–7 (C), 7–13 (D–E), and 5–6 (F), 5 (G), and 5–6 (H). Statistical significance was determined with the Student’s t test (C, D, F, G, H and I) and Mann–Whitney U test (E). *P<0.05, **P<0.01, and ***P<0.001.